Human physiological signals are perpetual. These signals are spontaneous or induced with molecular, cellular, neural and/or electrical origins. Many of these physiological signals manifest themselves in motions and movements in order to perform biologic and biochemical functions that sustain life. The better known motions are heartbeats, respiration and cardiopulmonary functions. But there are far subtler motions in all parts of a human body necessary and essential to support life. These physiological motions have been shown to follow certain non-linear dynamic laws, and possess fractal features and entrainment properties. These physiological motions are related to demographic factors, such as gender and age, and closely associated with the health or disease conditions of a human body. Physiological dynamics, while not always seen or felt by humans, are nonetheless always present and essential to life.
In particular, these constant physiological motions are present in the entire cardiovascular and circulatory system including arteries, veins and capillaries. Vasculature motions include vasomotion, vasodilation, vasoconstriction and vasospasm. These spontaneous motions in the vasculature system also lead to rhythmic changes in vessel diameter, wall thickness and vessel distensibility. Furthermore, blood vessels are elastic and characterized by certain viscoelastic properties. The dynamic and elastic nature of the vessels has particular effects on the success or failure of a therapeutic cardiovascular device.
Percutaneous access for various cardiovascular interventions is considered a safer and less invasive alternative to surgeries. This procedure has been developed since early 1950 and has now evolved into a popular and useful procedure treating a wide range of cardiovascular and vascular diseases including abdominal aortic aneurysm and heart valve repairs. Percutaneous access is either diagnostic or interventional (e.g. percutaneous coronary intervention, or PCI) with several possible access sites including artery, vein, femoral, radial or brachial locations. Each access site has its own advantages and limitations. The choice of the access site is often dependent on the disease condition, and on the preference of the practicing interventional cardiologist or radiologist. In all of these percutaneous interventions, there is a common denominator, i.e. hemostasis and healing of the vascular access site wound.
The preference in access site of a medical patient is geographically stratified and has evolved over time. Today, the angioplasty PCI procedure in the US is >95% femoral access while the radial access is favored in Europe and Asia at >70%. In the US, there has been a surge of radial access since 2007, mainly in response to the unabated bleeding and medical complications associated with femoral access. Reducing access site bleeding complications is the main reason cited for the conversion to radial access, even though radial access has its own limitations and disadvantages. Access site hemostasis and subsequent wound healing is important by itself as bleeding complications are often associated with serious human and economical costs; it is also important because it either contributes to the success of, or compromises, the underlying intervention.
Traditional design of hemostasis devices for percutaneous access site is based on a mechanistic barrier concept treating the “hole” of the injured vessel more like a hole in a leaking water pipe, i.e. treating the injured vessel as a stationary and motionless structure with constant dimensions. This barrier concept is reflected by many conventional terms such as “seal”, “plug”, or “clamping”. As such, current implant hemostasis devices provide a physical barrier to “plug” or “seal” the vascular “hole”, while current topical hemostasis devices provide a mechanical barrier to “clamp” the injured vessel from outward blood flow, and both as means of causing hemostasis. In reality, these actions only provide a resistive force to resist blood from gushing out after catheter removal, they do not cause hemostasis as defined by a cascade of time-dependent cellular processes of platelet aggregation, fibrin formation and subsequent wound healing. Furthermore, blood vessels are not a rigid stationary structure. Instead, blood vessels are soft, elastic and in various motions with constant changes in vessel diameter, wall thickness, and tone.
Because of the significant conceptual discrepancies, access site bleeding complications remain unabated after more than half a century. While the percutaneous technique has made significant advances, i.e. expanding to treating different types of diseases, increasing the size of the catheter and the aggressive use of anticoagulants, manual compression remains today as the “gold standard” in hemostasis management. Clinical experience and large scale statistics have amply validated that manual compression is inadequate and inapplicable in many situations and that the access site bleeding and vascular complications remain a significant medical and economic issue decades after the advent of the percutaneous procedure.
There are two types of topical hemostasis devices currently on the market addressing the percutaneous access site. One is the “topical patch” where a manufacturer claims to stop bleeding faster by visually judging no blood oozing out on the skin puncture surface. The other is the equivalent of manual compression, i.e. providing a compression force with a mechanical device or an instrument. The former (topical patch) provides a false sense of hemostasis as the injury site is under the skin on a breached vessel, and skin surface hemostasis is not an indication of the hemostasis of the injured vessel. Nor does the latter (manual or device compression) solve the problem. In fact, an exhaustive scientific literature search has shown that compression pressure does not cause platelet aggregation and fibrin formation. Not only does compression not promote the cellular processes of coagulation, the practice of strong and prolonged compression hinders cellular coagulation and causes additional injury and neurological damage to the patient. It is well documented that the initial seemingly successful hemostasis on the skin surface can turn into a serious bleeding medical event later in an unpredictable way. The unpredictable delayed hemostasis breach may manifest itself as life-threatening “invisible” retroperitoneal bleeding or a hematoma can be formed on locations other than the access site. These well-known clinical observations signify that the barrier concept has serious limitations. Today, there are no answers to these clinical observations, nor an effective way to predict, thus prevent, delayed bleeding complications.
This invention is the first to recognize that the dynamic and elastic nature of the injured vessel plays a key role in affecting and sustaining hemostasis in the vascular wound and surgical wound. This invention teaches that, while a barrier is immediately needed upon catheter removal or upon completion of a surgical intervention, to stop blood from gushing out, it is not enough to ensure hemostasis success and patient safety. This invention teaches how to use topical compressive force in an appropriate way to stop blood from gushing out upon catheter removal and, at the same time, sustain hemostasis and improve wound healing quality. This invention teaches how to timely affect and control vasculature motions to cause timely blood coagulation, how to sustain hemostasis until the fibrin clot has become stable, and how to improve wound healing quality. This invention teaches how to quench or reduce vasculature motions during the initial critical cellular phases of platelet activation, aggregation and fibrin matrix formation, as means to promote and sustain hemostasis.
This invention discloses a cooling element which provides an initial cooling profile on the injured skin surface to cause vasoconstriction and hemostasis, and a follow-on cooling profile to stabilize the injured vasculature structure to allow time for the fibrin clot to attain strength, thus reducing the potential for delayed hemostasis breach. This invention teaches a cooling profile to promote re-epithelialization, reduce scar formation and improve overall wound healing quality. This invention discloses a class of cooling materials for this application.
This invention discloses a compressive surface that is elastic to provide optimal compression, and comfort and safety to the patient. This invention discloses a compressive surface that is thermally conductive. This invention discloses a compressional force that is achieved through vertical displacement of the compression instrument, without causing lateral or transverse forces to adversely affect the wound.
This invention discloses how to use temperature to affect the injured vessel so that the vasculature structure is stabilized during the initial critical platelet aggregation and fibrin formation phase to allow a fibrin clot to attain strength to avoid unpredictable or delayed hemostasis breach. This invention discloses a therapeutic agent that affects the injured vessel so that the vasculature structure is stabilized during the initial critical platelet aggregation and fibrin formation phase to allow a fibrin clot to attain strength to avoid unpredictable or delayed hemostasis breach. This invention discloses a device and method to provide analgesic and anesthetic effect to the patient to reduce pain, reduce inflammation, reduce swelling, and reduce potential for infection. In sum, the invention device, in addition to providing an appropriate compressional force to resist blood outward flow, provides therapies to cause hemostasis, sustain hemostasis, and improve wound healing, thus achieving better clinical outcomes and reducing bleeding and reducing medical complications.